title: [Tumor necrosis factor alfa in cardiovascular diseases: molecular biology and genetics].
abstract: Cardiovascular diseases are a major public health problem globally. In 1997, cardiovascular disease caused 41% of deaths in the United States. It has been reported that about 60 million people in the United States have some form of cardiovascular disease. These entities are chronic conditions initiated by a dysregulation of the immune response. One gene and its protein product -tumor necrosis factor a (TNF-α)- a powerful pleiotropic cytokine with multiple cellular functions, plays a role in the inflammation, initiation, development, susceptibility, severity, and response to treatment, etc. of coronary artery disease (CAD). The focus of the present review is to summarize recent evidence showing the biological role of TNF-α in the initiation and progression of endothelial dysfunction and complications of atherosclerosis, and as a genetic variation of TNF-α confer susceptibility, severity, and treatment response in CAD: ST-segment elevation myocardial infarction and non-ST segment elevation myocardial infarction, unstable angina, and coronary restenosis.
authors.affiliation: Departamento de Biología Molecular, Instituto Nacional de Cardiología «Ignacio Chávez», México, D.F. dr.julian.ramirez.inv@gmail.com.
authors.forename: José Manuel
authors.initials: JM
authors.lastname: Fragoso Lona
authors.forename: Mónica
authors.initials: M
authors.lastname: Sierra Martínez
authors.forename: Gilberto
authors.initials: G
authors.lastname: Vargas Alarcón
authors.forename: Angélica
authors.initials: A
authors.lastname: Barrios Rodas
authors.forename: Julián
authors.initials: J
authors.lastname: Ramírez Bello
mesh_terms: D054058:Acute Coronary Syndrome / Q000209:etiology; D001669:Biochemical Phenomena; D002318:Cardiovascular Diseases / Q000209:etiology* / Q000235:genetics; D023903:Coronary Restenosis / Q000209:etiology; D006801:Humans; D058226:Plaque, Atherosclerotic / Q000209:etiology; D012422:Rupture, Spontaneous / Q000209:etiology; D015398:Signal Transduction; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology*
chemical_list: D014409:Tumor Necrosis Factor-alpha